Pines A, Kaplinsky N, Olchovsky D, Frankl O, Goldfarb D, Iaina A
Isr J Med Sci. 1985 Jan;21(1):50-2.
A case of anorexia nervosa in a 28-year-old woman with laxative abuse, hypopotassemia and severe metabolic acidosis, is described. The diagnosis of classical renal tubular acidosis, Type I, was confirmed by our inability to decrease urinary pH beyond 5.5 and to increase ammonia excretion during an ammonium chloride loading test. A bicarbonate loading test and normal plasma aldosterone with high renin activity excluded proximal renal tubular acidosis, hyporeninemic-hypoaldosteronemic renal tubular acidosis and Bartter's syndrome. The inability to increase ammonium excretion during severe metabolic acidosis following ammonium chloride loading did not favor the possibility of a transient physiological adaptation of ammoniagenesis at the tubular cell level, related to potassium depletion. Although mental disorder, laxative abuse, abstinence from food intake and severe potassium depletion intermingled in a vicious cycle, we assume that one of the following possibilities may explain the clinical presentation in our patient: either two separated and unrelated disorders, or laxative abuse as the cause of renal tubular acidification impairment.
本文描述了一名28岁患有神经性厌食症的女性,她滥用泻药,伴有低钾血症和严重代谢性酸中毒。在氯化铵负荷试验中,我们无法将尿液pH值降至5.5以下,也无法增加氨排泄,从而确诊为典型的I型肾小管酸中毒。碳酸氢盐负荷试验以及血浆醛固酮正常但肾素活性高,排除了近端肾小管酸中毒、低肾素性低醛固酮性肾小管酸中毒和巴特综合征。氯化铵负荷后严重代谢性酸中毒期间无法增加氨排泄,不支持肾小管细胞水平氨生成与钾缺乏相关的短暂生理适应的可能性。尽管精神障碍、滥用泻药、禁食和严重钾缺乏交织在一个恶性循环中,但我们认为以下可能性之一可以解释我们患者的临床表现:要么是两种分离且不相关的疾病,要么是滥用泻药导致肾小管酸化受损。